While many studies examine Nonalcoholic fatty liver disease (NAFLD), little is known about its progression to high-risk nonalcoholic steatohepatitis (NASH) in PsA patients. Shared disease mechanisms may explain the increased severity in PsA. This study involves two visits from PsA patients with NAFLD and active disease signs (e.g., swollen joint, enthesitis, or psoriatic plaque). It aims to assess the impact of biological therapies on liver disorders, joints, and skin in PsA patients.
Adults with diagnosis of PsA fulfilling the classification for PsA (CASPAR) criteria.
Patients with prior exposure to IL12/23i, IL-17i, JAKi, or TYK2i. Patients with exposure to more than 2 TNFi.
Evidence of other causes of chronic liver disease
Hepatitis B as defined as presence of hepatitis B surface antigen (HBsAg).
Previous or current infection with Hepatitis C as defined by presence of hepatitis C virus Abin serum (anti-HCV Ab).
Single group
Guselkumab
DrugThis is a longitudinal study consisting of a two-time visit by psoriatic arthritis patients. The aim of the study is to determine the effect of biological therapies in liver disorders in patients with psoriatic arthritis.
Change in NAFLD severity
Defined by MRI-PDFF responders (relative change in liver fat ≥30%) vs non-responders (relative change in liver fat \<30%) at Week 24.
Change from baseline in skin psoriasis severity
Defined by PASI90 (Psoriasis Area and Severity Index) response in patients with plaque psoriasis at baseline
Change in joint arthritis
Defined by change of 7.25 of DAPSA (Disease activity in Psoriatic Arthritis) from baseline in patients with at least 1 swollen joint at baseline.
Change in ALT Levels
Defined by at least 17 U/L in patients with elevated ALT at baseline (defined as ≥30 U/L).
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University of California, San Diego
Lead sponsor
Janssen Scientific Affairs, LLC
Collaborator
